COLLABORATIVE DIAGNOSIS:
Potential complications

bleeding related to:

decreased production of clotting factors associated with impaired liver function and decreased available vitamin K (can occur from malnutrition, antimicrobial therapy, and impaired absorption of vitamin K as a result of bile flow obstruction)

thrombocytopenia associated with hypersplenism (if venous congestion has resulted in splenomegaly, the spleen will destroy platelets faster than usual);

intrarenal vasoconstriction that may result from increased levels of certain renal arteriolar vasoconstrictors (e.g. angiotensin, endothelin), increased sympathetic nervous system activity, and impaired synthesis of renal vasodilators such as prostaglandin E2;

bleeding esophageal varices related to:

tortuosity and increased fragility of small vessels in the esophagus associated with portal hypertension

increase in abdominal girth (abdominal girth should be measured daily at the same time and in the same location on the abdomen with client in the same position)

dull percussion note over abdomen with finding of shifting dullness

presence of abdominal fluid wave

protruding umbilicus and bulging flanks.

Implement measures to reduce fluid volume excess, promote mobilization of fluid back into the vascular space, and prevent further third-spacing (see Diagnosis 2) in order to promote the resolution of ascites.

maintain an adequate fluid intake; if client is on a fluid restriction, maintain the maximum fluid intake allowed

administer albumin infusions if ordered to increase the intravascular volume

consult physician about reducing the dose of diuretic ordered if client loses more than 1 kg of weight/day (vigorous diuresis can reduce the intravascular volume enough to decrease renal blood flow and precipitate the hepatorenal syndrome)

instruct client to avoid activities such as straining to have a bowel movement, coughing, sneezing, and lifting heavy objects in order to prevent a sudden increase in intra-abdominal pressure; consult physician about an order for a laxative, antitussive, and/or decongestant if indicated

administer a nonselective beta-adrenergic blocker (e.g. propranolol, nadolol) to reduce portal pressure (a nitrate [e.g. isosorbide] may be given with the beta blocker to further reduce portal pressure)

turn client on side and suction as necessary to reduce risk of aspiration

maintain oxygen therapy as ordered

assist with administration of vasopressin or octreotide acetate (Sandostatin) if ordered to constrict splanchnic vessels and reduce blood flow to the portal vein (nitroglycerin is often given with vasopressin to lower portal pressure and also reduce the vasoconstrictor side effects of vasopressin)

prepare client for endoscopic sclerotherapy or ligation of varices if planned

dehydration/hypovolemia (reduced blood flow to the liver results in decreased detoxification of ammonia and other toxins)

consult physician about discontinuation of prescribed medications that are potential hepatotoxins (e.g. isoniazid, amiodarone, methyldopa, phenytoin) in order to prevent further liver damage

administer central nervous system depressants such as narcotics, sedative-hypnotics, and antianxiety agents with extreme caution (many of these agents are metabolized in the liver and may precipitate nonnitrogenous coma).

If signs and symptoms of hepatic encephalopathy occur:

maintain client on strict bed rest to reduce metabolic demands on the liver

ensure a high carbohydrate intake or administer intravenous glucose or tube feedings as ordered to provide a rapid energy source and decrease metabolism of endogenous proteins

administer enemas and/or cathartics as ordered to hasten expulsion of intestinal contents so that bacteria have less time to convert proteins to ammonia and other nitrogenous substances

administer the following medications if ordered:

antimicrobials that suppress activity of the intestinal flora (e.g. neomycin, metronidazole) to decrease protein breakdown in the intestine and subsequently reduce the formation of nitrogenous substances

lactulose to stimulate catharsis and create an acidic medium in the intestine (the acidity reduces bacterial growth and the resultant formation of nitrogenous substances and also traps ammonia in the colon by promoting the conversion of NH3to the poorly absorbed NH4)